OBJECTIVE -To examine whether decreased serum levels of adiponectin are an independent risk factor for the progression to type 2 diabetes in a Japanese population. RESEARCH DESIGN AND METHODS -The serum levels of adiponectin and tumor necrosis factor-␣ (TNF-␣) at baseline (from 1995 to 1997) were evaluated in 1,792 individuals (1,023 women and 769 men, aged 58.5 Ϯ 12.5 years) from a cohort population (n ϭ 3,706) of the Funagata study. Glucose tolerance was evaluated at baseline and also at 5-year follow-up examinations (n ϭ 978, follow-up rate, 54.6%) according to the 1985 World Health Organization criteria. The correlation of clinical traits with serum levels of adiponectin was examined. The association of the traits with the progression to type 2 diabetes at the 5-year follow-up was also examined.RESULTS -Among the traits examined, the correlation with aging was highest (r ϭ 0.312, P Ͻ 0.001). Eighteen subjects with normal glucose tolerance (NGT) developed diabetes, and 709 remained NGT at the 5-year follow-up examinations. The subjects who became diabetic had decreased serum levels of adiponectin (7.29 Ϯ 2.35 vs. 9.13 Ϯ 2.35 10 ϫ log g/ml, P ϭ 0.009). Multiple logistic regression analysis with age, sex, waist-to-hip ratio, and 2-h plasma glucose as the variables revealed that serum adiponectin level (odds ratio [per 0.1 log g/ml] 0.766, P ϭ 0.029) was an independent risk factor for the progression to type 2 diabetes. The subjects whose serum levels of adiponectin were in the lowest tertile were 9.320 times (95% CI 1.046 -83.1) more likely to develop diabetes than those in the highest tertile (P ϭ 0.046). CONCLUSIONS -Decreased serum adiponectin level is an independent risk factor for progression to type 2 diabetes. Diabetes Care 26:2015-2020, 2003A dipose tissue, in addition to its function as the major storage depot for lipids, plays active roles in normal metabolic homeostasis and in the development of several diseases, such as type 2 diabetes, dyslipidemia, and atherosclerosis (1,2). These roles are mediated by factors known as adipocytokines, which are secreted from adipose tissue (3). Among those factors, tumor necrosis factor-␣ (TNF-␣), leptin, and plasminogen-activator inhibitor type 1 (PAI-1) are well annotated, and the association of the dysregulated production of these factors with the pathophysiology of obesityrelated insulin resistance and thrombosis is well established (3-6).Adiponectin/ACRP30 is another adipocytokine, first identified in 1995 (7). The association of decreased plasma adiponectin levels with the presence of coronary artery disease (8) indicated the pathophysiological roles of adiponectin in the development of coronary artery disease. On the other hand, adiponectin's roles in stimulating -oxidation in muscle and decreasing insulin resistance in the liver (9) indicated its possible involvement in the development of type 2 diabetes. Indeed, its involvement was shown in many animal studies. Administration of adiponectin improved diabetes in mice (10,11), and adiponectin-knockout mice...
This study investigates whether urinary levels of pentosidine, pyrraline and acrolein adduct are increased in type 2 diabetes (DM), and whether these levels are correlated with glycemic control and clinical traits. Urinary levels of pentosidine, pyrraline and acrolein adduct in DM patients (n = 100) recruited from the outpatient clinic of our university hospital were compared with those of age- and sex-matched non-diabetic subjects (n = 50). The correlation of these urinary levels with the glycemic control and the clinical traits were examined. Furthermore, the influence of smoking habit on the levels of acrolein adduct was examined. Urinary levels of pentosidine, pyrraline and acrolein adduct were all significantly (p<0.001) higher in the DM group than in the non-DM group (pentosidine (log(pmol/mgCr)), 1.579 +/- 0.147 vs 1.427 +/- 0.142; pyrraline (log(nmol/mgCr)), 0.888 +/- 0.402 vs 0.581 +/- 0.336; acrolein adduct (log(nmol/mgCr)), 2.316 +/- 0.221 vs 2.051 +/- 0.201). Glycemic control parameters, such as fasting plasma glucose (FPG) and HbA1c, were significantly correlated with these urinary levels. Age was correlated with the urinary levels of pentosidine but not with those of pyrraline and acrolein adduct. The urinary albumin excretion rate did not correlate with any of these urinary levels. The levels of acrolein adduct were higher in the subjects with smoking habit than in those without the habit in the DM group as well as in the non-DM group (DM, 2.391 +/- 0.230 and 2.212 +/- 0.190, p=0.0004; Non-DM, 2.120 +/- 0.171 and 1.993 +/- 0.206, p=0.0503). The urinary levels of pentosidine, pyrraline and acrolein adduct were increased in DM and were significantly correlated with glycemic control levels. In addition, smoking habit seems to increase the urinary levels of acrolein adduct.
Background and Purpose-No large-scale study has ever compared the clinical and radiological features of lateral medullary infarction (LMI) and medial medullary infarction (MMI). The aim of this study was to investigate them through the use of cooperatively collected cases. Methods-Medical information on all patients from 1996 to 2000 with medullary infarction (MI) proven by brain MR images at 35 stroke centers in the Tohoku district, Japan, was collected, and their clinical and radiological features were analyzed. Results-A total of 214 cases of MI were registered. They included 167 cases (78%) of LMI, 41 (19%) of MMI, and 6 (3%) of LMI plus MMI. The mean age of onset and the male-to-female ratio were 60.7 years and 2.7:1 in LMI and 65.0 years and 3.6:1 in MMI, respectively. The middle medulla was most frequently affected in LMI, and the upper medulla was most frequently affected in MMI. Dissection of the vertebral artery was observed in 29% of LMI and 21% of MMI. Prognosis, assessed by the Barthel Index, was favorable in both LMI and MMI. Diabetes mellitus was more frequently associated with MMI than with LMI. Conclusions-The present study surveyed a large number of MI cases and revealed that (1) the mean age of onset of MMI is higher than that of LMI, (2) the dissection of the vertebral artery is an important cause not only of LMI but also of MMI, and (3) diabetes mellitus is frequently associated with MMI.
OBJECTIVE -Despite a large number of studies, no association of the Trp64Arg polymorphism of the  3 -adrenergic receptor gene with obesity and type 2 diabetes has yet to be clearly elucidated. We examined the associations in a large population-based sample.RESEARCH DESIGN AND METHODS -A total of 1,685 subjects (935 women and 750 men, aged 58.7 Ϯ 12.4 years) from a cohort population (n ϭ 3,706) of the Funagata Diabetes Study were divided into three groups according to genotypes: Trp/Trp (n ϭ 1,155), Trp/Arg (n ϭ 486), and Arg/Arg (n ϭ 44). Glucose tolerance was diagnosed according to the 1985 World Health Organization criteria. Subjects who had a BMI Ն30 kg/m 2 were considered obese. Associations with the traits related to obesity, diabetes, hypertension, and dyslipidemia were also examined. The 2 test and analysis of variance were used for the association studies and to assess the differences in the traits' values, respectively.RESULTS -More subjects with genotype Arg/Arg were obese and had diabetes (13.6% for each) than those with genotype Trp/Trp (3.29%, P Ͻ 0.001; and 4.16%, P ϭ 0.007, respectively) or genotype Trp/Arg (2.06%, P Ͻ 0.001; and 5.97%, P ϭ 0.051, respectively). No significant differences in the frequencies of occurrence of these conditions were observed between genotypes Trp/Arg and Trp/Trp. Traits related to obesity, such as percent body fat (28.82 Ϯ 7.95 vs. 25.93 Ϯ 7.21, P ϭ 0.038) and BMI (25.07 Ϯ 3.84 vs. 23.63 Ϯ 3.18, P ϭ 0.018), were higher in the genotype Arg/Arg than in the genotype Trp/Trp groups.CONCLUSIONS -Genotype Arg/Arg, but not Trp/Arg, of the  3 -adrenergic receptor was associated with both obesity and type 2 diabetes in a large Japanese sample.
Obesity, which is a risk factor for various disorders including type 2 diabetes, hypertension, cancer, and cardiovascular disease, is one of the most common disorders in clinical practice worldwide and, thus, a global public health problem. It has been reported that the occurrence of obesity is determined by both environmental and genetic factors [1]. Increased energy intake and decreased physical activity are such envi- Abstract. The association of the FTO gene polymorphism, rs9939609, with obesity was examined using the population of the Takahata study (n (M/F): 2,639 (1,168 / 1,470); age: 63.0 ± 10.2 years), a Japanese community-based study. The effects of lifestyle-related factors, including nutritional intake and physical activities, on the association were also examined. Body mass index (BMI) was significantly associated with the FTO gene polymorphism (p<0.001). A case-control association study of the FTO gene polymorphism with obesity using multiple logistic regression analysis showed a significant association of the genotype AA (odds ratio, 1.53 [95% confidential interval, 1.04-2.24]) after adjustment for age and gender. Analysis to examine the differences in lifestyle-related factors among the genotype groups showed a significant difference in the energy expenditure for moderate to high-intensity physical activity (PA) (≥ 3.0 METs) (p=0.012) with a significant decrease toward the genotype AA (p=0.027). The effect of energy expenditure for moderate to high-intensity PA on the association of the polymorphism with obesity was then examined using study groups stratified based on the energy expenditure for moderate to high-intensity PA (Low-PA and High-PA). The BMI was significantly higher in the genotype AA in the Low-PA group (p=0.016) but not in the High-PA group (p=0.103). Furthermore, the genotype AA was significantly associated with obesity (odds ratio, 2.39 [95% confidential interval, 1.19-4.80]) in the Low-PA group but not in the High-PA group (p=0.650). The FTO gene, rs9939609, was associated with obesity, and the association was evident in subjects with low-PA, suggesting a PA-dependent association.
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